In gastrointestinal stromal tumors (GIST), knockdown of PD-L1 inhibited the expression level of PI3K, p-PI3K, and p-AKT, whereas the alteration of PI3K/AKT/mTOR pathway blocked PD-1/PD-L1 and attenuated apoptosis of CD8+ T cells.510 Activation of the PI3K/AKT pathway mediates PD-L1-induced P-gp upregulation in GC drug resistance.511 Wang et al.416 reported that autophagy inhibition increased PD-L1 expression by increasing the p62/SQSTM1 level and activating nuclear NF-κB in GC, which can be abolished by p62/SQSTM1 inhibition or NF-κB knock down. This evidence concerns the gene CD8A and gastrointestinal stromal tumor.